title: [Study on mechanism of thyroid cytotoxicity of ammonium perchlorate].
abstract: OBJECTIVE
  To investigate the mechanism of thyroid cytotoxicity mechanism of ammonium perchlorate (AP).
  
  
  METHODS
  Thyroid cells were cultured in vitro to a certain stage and then exposed to AP (0, 5, 10, 20, 40, and 60 mmol/L) in culture solution; the cultured cells and supernatant were collected. Cell viability was measured by MTT assay; cell apoptosis was determined by flow cytometry; the concentration of thyroglobulin was measured by enzyme-linked immunosorbent assay; the lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA) level, and so on were measured by colorimetry.
  
  
  RESULTS
  The cells exposed to 60 mmol/L AP for 12, 24, 48, and 72 h had cell viabilities of 74.93%, 42.26%, 2.66%, and 0.99%, respectively, and the cells exposed to 40 mmol/L AP for 24, 48, and 72 h had cell viabilities of 73.15%, 30.91%, and 3.03%, respectively, all significantly lower than that of the control group (100%)(P < 0.05 or P < 0.01). The overall apoptosis rate of all AP-exposed cells was significantly higher than that of the control group; the cells exposed to 20, 40, and 60 mmol/L AP had early apoptosis rates of 15.70%, 15.84%, and 16.96%, respectively, significantly higher than that of the control group (9.54%)(P < 0.05 or P < 0.01); the cells exposed to 60 mmol/L AP had a late apoptosis rate of 16.54%, significantly higher than that of the control group (6.11%)(P < 0.05 or P < 0.01). The cells exposed to 40 mmol/L AP had a significantly higher LDH activity than the control group (0.70 U/ml vs 0.55 U/ml, P < 0.01). The cells exposed to 5 mmol/L AP had a significantly higher MDA level than the control group (1.08 mmol/L vs 2.36 mmol/L, P < 0.05).
  
  
  CONCLUSIONS
  AP can markedly change the cell morphology and decrease the cell viability of thyroid cells, which may be because AP inhibits cell proliferation, induces cell apoptosis, and destroys cell membranes. However, AP does not result in significant oxidative damage to thyroid cells.
authors.affiliation: Public Health School, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Liu
authors.forename: Miao-hong
authors.initials: MH
authors.lastname: Ding
authors.forename: Rao
authors.initials: R
authors.lastname: Zhang
authors.forename: Hong-xia
authors.initials: HX
authors.lastname: Chen
authors.forename: Xing-xing
authors.initials: XX
authors.lastname: Zhou
authors.forename: Hui-fang
authors.initials: HF
authors.lastname: Xu
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Kai-liang
authors.initials: KL
authors.lastname: Peng
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D006801:Humans; D018384:Oxidative Stress; D010472:Perchlorates / Q000633:toxicity*; D000644:Quaternary Ammonium Compounds / Q000633:toxicity*; D013954:Thyroglobulin / Q000378:metabolism; D013961:Thyroid Gland / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology
chemical_list: D010472:Perchlorates; D000644:Quaternary Ammonium Compounds; D013954:Thyroglobulin; C053506:ammonium perchlorate